Article

Striatal amphetamine-induced dopamine release in patients with schizotypal personality disorder studied with single photon emission computed tomography and [123I]iodobenzamide.

Department of Psychiatry, Columbia University, and New York State Psychiatric Institute, New York, 10032, USA.
Biological Psychiatry (Impact Factor: 9.47). 06/2004; 55(10):1001-6. DOI: 10.1016/j.biopsych.2004.01.018
Source: PubMed

ABSTRACT Previous imaging studies demonstrated that schizophrenia is associated with increased amphetamine-induced dopamine (DA) release in the striatum, most pronounced during episodes of illness exacerbation. Schizotypal personality disorder (SPD) is a schizophrenia spectrum disorder, genetically related to schizophrenia. The goal of this study was to investigate striatal DA function in patients with SPD.
In our study, 13 SPD patients and 13 matched healthy control subjects underwent single photon emission computed tomography (SPECT) scan during bolus plus constant infusion of the D2/3 radiotracer [123I]iodobenzamide (IBZM). Striatal specific to nonspecific equilibrium partition coefficient (V(3)") was measured at baseline and following amphetamine administration (.3 mg/kg).
No significant differences were observed in baseline V(3)" between groups. Amphetamine induced a larger decrease in [123I]IBZM V(3)" in SPD patients (-12 +/- 5%) compared with control subjects (-7 +/- 5%, p =.03).
The reduction in [123I]IBZM V(3)" induced by amphetamine in SPD was similar to that observed in remitted schizophrenia patients (-10 +/- 9%, n = 17), but significantly lower than that observed during illness exacerbation (-24 +/- 13%, n = 17). This suggests that DA dysregulation in schizophrenia spectrum disorders might have a trait component, present in remitted patients with schizophrenia and in SPD, and a state component, associated with psychotic exacerbations but not SPD.

0 Bookmarks
 · 
86 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Schizotypy refers to a constellation of personality traits that are believed to mirror the subclinical expression of schizophrenia in the general population. Evidence from pharmacological studies indicates that dopamine (DA) is involved in the etiology of schizophrenia. Based on the assumption of a continuum between schizophrenia and schizotypy, researchers have begun investigating the association between DA and schizotypy using a wide range of methods. In this article, we review published studies on this association from the following areas of work: (1) experimental investigations of the interactive effects of dopaminergic challenges and schizotypy on cognition, motor control, and behavior (2), dopaminergically supported cognitive functions (3), studies of associations between schizotypy and polymorphisms in genes involved in dopaminergic neurotransmission, and (4) molecular imaging studies of the association between schizotypy and markers of the DA system. Together, data from these lines of evidence suggest that DA is important to the expression and experience of schizotypy and associated behavioral biases. An important observation is that the experimental designs, methods, and manipulations used in this research are highly heterogeneous. Future studies are required to replicate individual observations, to enlighten the link between DA and different schizotypy dimensions (positive, negative, cognitive disorganization), and to guide the search for solid DA-sensitive behavioral markers. Such studies are important in order to clarify inconsistencies between studies. More work is also needed to identify differences between dopaminergic alterations in schizotypy compared to the dysfunctions observed in schizophrenia.
    Frontiers in Psychiatry 12/2014; 5:184. DOI:10.3389/fpsyt.2014.00184
  • [Show abstract] [Hide abstract]
    ABSTRACT: An increased risk for psychosis is observed in people with hearing impairment. According to the social defeat hypothesis, the long-term experience of exclusion leads to enhanced baseline activity and/or sensitization of the dopamine system and puts the individual at increased risk for psychosis.
    JAMA Psychiatry 10/2014; 71(12). DOI:10.1001/jamapsychiatry.2014.1325 · 12.01 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Schizophrenia is an illness with a remarkably complex symptom presentation that has thus far been out of reach of neuroscientific explanation. This presents a fundamental problem for developing better treatments that target specific symptoms or root causes. One promising path forward is the incorporation of computational neuroscience, which provides a way to formalize experimental observations and, in turn, make theoretical predictions for subsequent studies. We review three complementary approaches: (a) biophysically based models developed to test cellular-level and synaptic hypotheses, (b) connectionist models that give insight into large-scale neural-system-level disturbances in schizophrenia, and (c) models that provide a formalism for observations of complex behavioral deficits, such as negative symptoms. We argue that harnessing all of these modeling approaches represents a productive approach for better understanding schizophrenia. We discuss how blending these approaches can allow the field to progress toward a more comprehensive understanding of schizophrenia and its treatment.
    01/2015; DOI:10.1177/2167702614562041

Full-text

Download
7 Downloads
Available from
Jul 18, 2014